Prostate cancer (PrCa) is the second leading cause of cancer related death in North American men. In the majority of cases, PrCa becomes androgen-independent (Al) or hormone refractory. Progression to Al PrCa is multi-factorial and can be attributed to activation of pro-survival cell signaling by circulating growth factors, aberrant androgen receptor (AR) transcription and evasion of apoptosis. We have shown that the oncoprotein, Beta-catenin, can alter AR transcription and potentially contribute towards aberrant growth during Al PrCa. We have also shown that the tumour suppressor, PTEN, can negatively regulate Beta-catenin/Tcf signaling. Using both loss and gain of function systems we proposed to further evaluate the role of Beta-catenin in PrCa. Specifically, a prostate specific PTEN knock-out mouse will allow us to evaluate expression and distribution of Beta-catenin and molecules known to regulate its activity. We will also employ the use of LNCaP PrCa cells stably transfected with PTEN under an inducible Tet regulated promoter. These cells will be assessed for growth and PSA secretion in tumors carried as xenografts. These novel in vivo tools will allow understanding to the role of Beta-catenin has in Al PrCa.